Ailmemts & Remedies

Takotsubo cardiomyopathy

  1. Other Names: Broken-heart syndrome, Transient apical ballooning syndrome, Apical ballooning cardiomyopathy,Stress-induced cardiomyopathy, Gebrochenes-Herz-Syndrom, and Stress cardiomyopathy.
    Takotsubo cardiomyopathy is a type of non-ischaemic cardiomyopathy in which there is a sudden temporary weakening of the myocardium. Because this weakening can be triggered by emotional stress, It occurs as the response of the heart to sudden, intense emotional stress such as the death of a spouse; rejection at the workplace; acute fear; or uncontrolled anger. These intense emotions can cause immediate breathlessness or strokes. The broken heart can occur simultaneously or a few minutes later. Stress cardiomyopathy is a well-recognized cause of acute heart failure, lethal ventricular arrhythmias, and ventricular rupture.


Around ten years ago, there were a few high profile deaths in young people. They were diagnosed as having died from a “broken heart”. Now, a broken heart or stunned myocardium syndrome is a documented condition.
Takotsubo cardiomyopathy or Broken heart syndrome symptoms can mimic a heart attack.The symptoms are similar to a heart attack – chest pain, sweating, giddiness or dizziness, nausea, vomiting, weakness and palpitations. Blood pressure may drop. Heart failure may develop.

Any long-lasting or persistent chest pain could be a sign of a heart attack, so it’s important to take it seriously and call your doctor if you experience chest pain.

The exact cause of Takotsubo cardiomyopathy is not very clear. It is thought that a surge of stress hormones, such as adrenaline, might temporarily damage the hearts of some people. How these hormones might hurt the heart or whether something else is responsible isn’t completely clear. A temporary constriction of the large or small arteries of the heart may play a role.

Takotsubo cardiomyopathy is often preceded by an intense physical or emotional event. Some potential triggers are:

*News of an unexpected death of a loved one
*A frightening medical diagnosis
*Domestic abuse
*Losing a lot of money
*Natural disasters
*A surprise party
*Having to perform publicly
*Job loss
*Physical stressors, such as an asthma attack, a car accident or major surgery

It’s also possible that some drugs, rarely, may cause broken heart syndrome by causing a surge of stress hormones. Drugs that may contribute to broken heart syndrome include:

*Epinephrine (EpiPen, EpiPen Jr), which is used to treat severe allergic reactions or a severe asthma attack
*Duloxetine (Cymbalta), a medication given to treat nerve problems in people with diabetes, or as a treatment for depression
*Venlafaxine (Effexor XR), which is a treatment for depression
*Levothyroxine (Synthroid, Levoxyl), a drug given to people whose thyroid glands don’t work properly
Differances between Takotsubo cardiomyopathy and hear attack are:

Heart attacks are generally caused by a complete or near complete blockage of a heart artery. This blockage is due to a blood clot forming at the site of narrowing from fatty buildup (atherosclerosis) in the wall of the artery. In Takotsubo cardiomyopathy, the heart arteries are not blocked, although blood flow in the arteries of the heart may be reduced.
Takotsubo cardiomyopathy or Transient apical ballooning syndrome is found in 1.7–2.2% of patients presenting with acute coronary syndrome. While the original case studies reported on individuals in Japan, Takotsubo cardiomyopathy has been noted more recently in the United States and Western Europe. It is likely that the syndrome went previously undiagnosed before it was described in detail in the Japanese literature.

The diagnosis of Takotsubo cardiomyopathy may be difficult upon presentation. The ECG findings are often confused with those found during an acute anterior wall myocardial infarction. It classically mimics ST-segment elevation myocardial infarction, and is characterised by acute onset of transient ventricular apical wall motion abnormalities (ballooning) accompanied by chest pain, dyspnea, ST-segment elevation, T-wave inversion or QT-interval prolongation on ECG. Elevation of myocardial enzymes is moderate at worst and there is absence of significant coronary artery disease.

The diagnosis is made by the pathognomonic wall motion abnormalities, in which the base of the left ventricle is contracting normally or is hyperkinetic while the remainder of the left ventricle is akinetic or dyskinetic. This is accompanied by the lack of significant coronary artery disease that would explain the wall motion abnormalities. Although apical ballooning has been classically described as the angiographic manifestation of takotsubo, it has been shown that left ventricular dysfunction in this syndrome includes not only the classic apical ballooning, but also different angiographic morphologies such as mid-ventricular ballooning and rarely local ballooning of other segments.

The ballooning patterns were classified by Shimizu et al. as takotsubo type for apical akinesia and basal hyperkinesia, reverse takotsubo for basal akinesia and apical hyperkinesia, mid-ventricular type for mid-ventricular ballooning accompanied by basal and apical hyperkinesia and localised type for any other segmental left ventricular ballooning with clinical characteristics of takotsubo-like left ventricular dysfunction.

The ECG changes are atypical, with imprecise changes in the ST segment and T waves. They are “suspicious of but non conclusive” of myocardial infraction. Blood tests for the enzyme creatine kinase and proteins troponin should be done. These are elevated in a heart attack. In a stunned heart, these results too are inconclusive. The echocardiogram is the clincher. The heart is ballooned out. This change occurs typically at the apex of the heart. It is important to make a distinction between heart attack and takotsubo as the medication is different.

The treatment for takotsubo is mainly supportive. Medication is given to remove fluid from the lungs and prevent clots. Recovery occurs within a few days.

About two per cent of people who were thought to have a heart attack actually had broken hearts. In the case of women, this increases to seven per cent. Women, mainly menopausal ones (60-75 years), have “broken hearts” eight to nine times more often than men. Some people are genetically prone to “broken hearts.” Depression plays a role in susceptibility to this condition. Recurrences can occur in 10 per cent of people.

People who are in poor physical condition do not need severe emotional stress to suffer a broken heart. An episode may be precipitated by a minor event like rejection, or even a lecture or talk before an audience.

In order to never develop this condition; it is important to develop metal and physical toughness. Walking for 40-60 minutes a day at a brisk pace exposes the heart to small doses of adrenaline and nor adrenaline in a controlled manner. The heart gets conditioned and is immune to sudden chemical surges. Meditation and yoga provide calmness and the mental strength to cope with good days and bad.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.


News on Health & Science

Federal Panel to Review Use of Artery Device

PFIZER’S decision last weekend to abandon a promising cholesterol drug is but the latest recent setback as the health care industry continues its assault on cardiovascular disease, which has remained the leading cause of death and disability in Western societies since World War I……… & see

Another reminder of the difficulties will come this week in Washington. Thursday will be the first of two days of hearings by a federal advisory panel that is expected to recommend stricter regulation on the use of drug-coated stents, the medical device industry’s most popular tool for dealing with clogged heart arteries.

The panel will weigh evidence that the stents, which were developed to keep coronary arteries open after they have been cleared of plaque, can in some cases cause fatal blood clots months or even years after they have been put in patients.

“From where we sit, there are more questions than answers,” said Dr. Daniel G. Schultz, director of the Center for Devices and Radiological Health at the Food and Drug Administration, which is holding the hearings.

Wall Street is uneasy, too. The nation’s market leader in stents, Boston Scientific, whose stock was struggling under the weight of the company’s $27 billion takeover of Guidant in April, has experienced an additional 7 percent stock decline in the last three months  largely on rising concern among doctors and consumers about the long-term clotting risks.

The nation will spend close to $258 billion treating cardiovascular diseases this year, according to the American Heart Association, including $50 billion on devices and drugs.

But drug and device companies face a shifting landscape in which the traditional image of the heart and circulatory system   pipes and pumps where any clogging is a threat   has been replaced by a far more complicated picture. It is now clear that the human circulatory system can adapt to some types of clogging, but that patients can be killed without warning by the rupture of “vulnerable plaque”: fatty deposits containing a stew of cells that can cause rapid formation of a clot.

So far, though, there is no sure way to locate which plaques are about to rupture. Nor is there a proven drug or device for preventing their formation, dissolving them or sealing them off.

“Technology is pushing against the limits of our knowledge, and we are finding that to a certain extent, things are more complicated than we thought,   said Dr. Barry T. Katzen, director of the Baptist Cardiac and Vascular Institute at Baptist Hospital of Miami.

There are numerous forms of cardiovascular disease, which causes or contributes to the death of 2,500 Americans every day, according to the American Heart Association. While heart attack may be the most obvious dire outcome, symptoms as diverse as swelling of the feet, sexual dysfunction, stroke, kidney failure and chest pains are all common.

The death rate has been falling since the 1960s, a trend driven by the decline of smoking and more attention to healthier diets and lifestyles. But medical technology like heart pacemakers and defibrillators; blood-thinning and anti-clotting.
drugs; and, more recently, the cholesterol-fighting statin drugs have all helped, too.

Pfizer was chasing a potential blockbuster vision of reversing the progression of heart disease. Its drug torcetrapib stimulates production of a fat-grabbing protein   high-density lipoprotein, or HDL, the so-called good cholesterol. High levels of HDL can reverse plaque accumulation.

In theory, drug companies that are already working on closely related HDL stimulators may achieve torcetrapib’s benefits without its dangerous side effect of raising blood pressure. But Dr. Steven E. Nissen, chairman of cardiovascular medicine at the Cleveland Clinic, who was the lead investigator on an early clinical trial that highlighted the promise of torcetrapib, said researchers might now have difficulty enrolling patients in trials of related drugs.   It might kill the class,  he said.

Stents, meanwhile, are frequently used to relieve the disabling discomfort of angina rather than treat acute heart disease. They were introduced in the 1990s as an enhancement to angioplasty, a procedure in which a tiny balloon is inflated inside a blockage in a blood vessel to create a broader channel for blood flow. Bare-metal stents halved the frequency with which coronary arteries quickly clogged up again at the angioplasty site to about 20 percent.

Drug-coated stents, introduced in the United States in 2003, cut the reblockage frequency in half again and quickly grabbed close to 90 percent of the market because they saved patients the costs and risks of repeat procedures. Boston Scientific’s Taxus and Johnson & Johnson Cypher are the only drug-coated devices currently approved for sale, although Medtronic recently asked the F.D.A. to approve its Endeavor stent, and several other potential competitors are also developing products.

But now stent sales are falling in the United States and doctors report numerous calls from patients wondering whether the drug-coated devices are ticking time bombs. The risk may be slight, but it adds up to tens of thousands of heart attacks annually, because 600,000 Americans now receive coronary stents each year. And research suggests that such heart attacks kill as many as half of the patients who suffer them.

So far, the added risks of late clotting appear to balance the added risks of repeat procedures for bare-metal stents. That leaves unsettled the question of which device — the drug-coated or the bare-metal stent — might be safer in the long run.

One contentious issue the F.D.A. panel plans to discuss is the risk, benefit and cost of keeping patients indefinitely on a daily diet of aspirin and the anticlotting drug Plavix, to reduce the late clotting risk. Wall Street will also be watching closely to find out whether the panelists urge the F.D.A. to discourage the widespread “off-label” use of drug-coated devices in groups of patients who are in poorer health than those studied in the clinical trials.

One suggestion has been that the F.D.A. may require longer-term safety data for new stents. Because many of the new designs have features and early data suggesting they may be safer than Taxus or Cypher, however, some experts believe the F.D.A. will end up requiring more rigorous follow-up studies, rather than delay their entry into the market.

The new designs point to a persistent challenge for medical device regulators. Will changing technology render obsolete much of the safety data doctors are clamoring for about today’s devices before it can be compiled?

Source:New York Times